Watkins J B, Dykstra T P
Drug Metab Dispos. 1987 Mar-Apr;15(2):177-83.
Hepatic clearance and biliary excretion of model substrates for each of four carrier-mediated transport systems were studied in male Sprague-Dawley rats treated 28 days earlier with 45 mg/kg streptozotocin iv to induce uncontrolled insulin-deficient diabetes. Diabetic rats exhibited hyperglycemia (560 mg/dl), polyuria (160 ml/24 hr), polyphagia, polydipsia, and generalized myopathy. The plasma disappearance, biliary excretion, and elimination half-life of the anionic dye phenol red was unchanged in diabetic rats, but total clearance of phenol red was increased. Conjugation of phenol red with glucuronic acid appeared to be increased in diabetic rats, whereas acetylation of procainamide ethobromide was decreased. Plasma elimination and total clearance of cationic procainamide ethobromide, uncharged ouabain, and the bile acid taurocholate were significantly increased in diabetic animals. Biliary excretion of these three compounds was only slightly elevated in the first 15 min after administration and was decreased after 1 hr. Biliary and total systemic clearance were also increased from 2-3-fold for procainamide ethobromide, ouabain, and taurocholate. These changes in clearance are predominantly due to the 2-5-fold increase in steady state volume of distribution. Basal bile flow rates were increased by 62% after the induction of diabetes to 88 microliter/min/kg. Diabetic rats secreted higher levels of bile acids, cholesterol, and phospholipids into bile. These data indicate that long term insulin-dependent diabetes does alter hepatic excretory function.
在28天前经静脉注射45mg/kg链脲佐菌素以诱导胰岛素缺乏性糖尿病的雄性Sprague-Dawley大鼠中,研究了四种载体介导转运系统各自的模型底物的肝清除率和胆汁排泄。糖尿病大鼠表现出高血糖(560mg/dl)、多尿(160ml/24小时)、多食、多饮和全身性肌病。阴离子染料酚红的血浆消失、胆汁排泄和消除半衰期在糖尿病大鼠中未发生变化,但酚红的总清除率增加。糖尿病大鼠中酚红与葡萄糖醛酸的结合似乎增加,而普鲁卡因胺乙溴化物的乙酰化减少。糖尿病动物中阳离子普鲁卡因胺乙溴化物、中性哇巴因和胆汁酸牛磺胆酸盐的血浆消除和总清除率显著增加。这三种化合物的胆汁排泄在给药后的最初15分钟内仅略有升高,1小时后降低。普鲁卡因胺乙溴化物、哇巴因和牛磺胆酸盐的胆汁清除率和全身总清除率也增加了2-3倍。清除率的这些变化主要是由于稳态分布容积增加了2-5倍。糖尿病诱导后,基础胆汁流速增加62%,达到88微升/分钟/千克。糖尿病大鼠向胆汁中分泌更高水平的胆汁酸、胆固醇和磷脂。这些数据表明长期胰岛素依赖型糖尿病确实会改变肝脏的排泄功能。